Ever since the discovery of active and adequate brown fat depots in adult humans, non-shivering thermogenesis (NST) function of brown adipose tissue (BAT), where oxidation of tissue-stored fats is uncoupled from ATP synthesis and instead used to generate heat for the body, has become a promising avenue for metabolic disease research in the last decade. As BAT utilizes its stored fats for the purpose of generating heat for the body, it also maintains a stable energy storage in the form of fats within brown adipocytes. To prevent replenishment of these fat stores, upon cold stimuli, BAT picks up additional glucose from plasma to be converted into storage triglycerides via de novo lipogenesis (DNL), alongside taking up additional lipids also from plasma. If the cold stimuli are long enough, the same phenomena are observed in white adipose tissue (WAT) as well via a process called browning. These trends make BAT, NST and WAT browning exciting avenues for metabolic disease research targeting type 2 diabetes and obesity, alongside fatty liver diseases and other metabolic conditions. ChREBP, as a glycolytic and lipogenic transcription factor identified more than a decade ago, has been established to be the main driver of DNL in adipocytes and thus has important roles in the processes observed in BAT and WAT during NST and browning, which can have far-reaching implications. The present thesis work evaluates effects and necessity of ChREBP function by analysing its organ-specific roles during metabolic adaptation to cold, in liver, BAT, and WAT via gene expression, protein expression, and tissue uptake data obtained from murine cohorts with ChREBP availability versus deletion, housed under different ambient temperatures.